Bone Morphogenetic Proteins
Bone Morphogenetic Protein 2
Bone Morphogenetic Protein 4
Bone Morphogenetic Protein 7
Bone Morphogenetic Protein Receptors, Type I
Bone Morphogenetic Protein Receptors
Bone Morphogenetic Protein 6
Bone Morphogenetic Protein Receptors, Type II
Bone and Bones
Bone Morphogenetic Protein 5
Bone Morphogenetic Protein 3
Bone Morphogenetic Protein 15
Bone Morphogenetic Protein 1
Transforming Growth Factor beta
Growth Differentiation Factor 2
Receptors, Growth Factor
Growth Differentiation Factors
Growth Differentiation Factor 5
Gene Expression Regulation, Developmental
Growth Differentiation Factor 9
Activin Receptors, Type I
Growth Differentiation Factor 6
Intercellular Signaling Peptides and Proteins
Activin Receptors, Type II
Bone Marrow Cells
Inhibitor of Differentiation Protein 1
Smad Proteins, Receptor-Regulated
In Situ Hybridization
MSX1 Transcription Factor
Core Binding Factor Alpha 1 Subunit
Reverse Transcriptase Polymerase Chain Reaction
Gene Expression Regulation
Mesenchymal Stromal Cells
Receptors, Transforming Growth Factor beta
Molecular Sequence Data
Bone Marrow Transplantation
Fibroblast Growth Factors
Embryonic Stem Cells
Amino Acid Sequence
Limb Deformities, Congenital
Antimicrobial Cationic Peptides
Receptors, Cell Surface
Extracellular Matrix Proteins
Transforming Growth Factor beta1
Bone Demineralization Technique
Inhibitor of Differentiation Proteins
Growth Differentiation Factor 10
Disease Models, Animal
SOX9 Transcription Factor
Collagen Type I
Myocytes, Smooth Muscle
Promoter Regions, Genetic
Protein Structure, Tertiary
Fibroblast Growth Factor 8
Culture Media, Conditioned
Transforming Growth Factor beta3
Gene Expression Profiling
Transforming Growth Factor beta2
Ectopic bone morphogenetic proteins 5 and 4 in the chicken forebrain lead to cyclopia and holoprosencephaly. (1/42)Proper dorsal-ventral patterning in the developing central nervous system requires signals from both the dorsal and ventral portions of the neural tube. Data from multiple studies have demonstrated that bone morphogenetic proteins (BMPs) and Sonic hedgehog protein are secreted factors that regulate dorsal and ventral specification, respectively, within the caudal neural tube. In the developing rostral central nervous system Sonic hedgehog protein also participates in ventral regionalization; however, the roles of BMPs in the developing brain are less clear. We hypothesized that BMPs also play a role in dorsal specification of the vertebrate forebrain. To test our hypothesis we implanted beads soaked in recombinant BMP5 or BMP4 into the neural tube of the chicken forebrain. Experimental embryos showed a loss of the basal telencephalon that resulted in holoprosencephaly (a single cerebral hemisphere), cyclopia (a single midline eye), and loss of ventral midline structures. In situ hybridization using a panel of probes to genes expressed in the dorsal and ventral forebrain revealed the loss of ventral markers with the maintenance of dorsal markers. Furthermore, we found that the loss of the basal telencephalon was the result of excessive cell death and not a change in cell fates. These data provide evidence that BMP signaling participates in dorsal-ventral patterning of the developing brain in vivo, and disturbances in dorsal-ventral signaling result in specific malformations of the forebrain. (+info)
Early embryonic lethality in Bmp5;Bmp7 double mutant mice suggests functional redundancy within the 60A subgroup. (2/42)Members of the BMP family of signaling molecules display a high conservation of structure and function, and multiple BMPs are often coexpressed in a variety of tissues during development. Moreover, distinct BMP ligands are capable of activating common pathways. Here we describe the coexpression of two members of the 60A subfamily of BMPs, Bmp5 and Bmp7, at a number of different sites in the embryo from gastrulation onwards. Previous studies demonstrate that loss of either Bmp5 or Bmp7 has negligible effects on development, suggesting these molecules functionally compensate for each other at early stages of embryonic development. Here we show this is indeed the case. Thus we find that Bmp5;Bmp7 double mutants die at 10.5 dpc and display striking defects primarily affecting the tissues where these factors are coexpressed. The present analysis also uncovers novel roles for BMP signaling during the development of the allantois, heart, branchial arches, somites and forebrain. Bmp5 and Bmp7 do not appear to be involved in establishing pattern in these tissues, but are instead necessary for the proliferation and maintenance of specific cell populations. These findings are discussed with respect to potential mechanisms underlying cooperative signaling by multiple members of the TGF-beta superfamily. (+info)
Molecular characterization and phylogenetic analysis of SpBMP5-7, a new member of the TGF-beta superfamily expressed in sea urchin embryos. (3/42)TGF-beta ligands are probably pan-bilaterian in phylogenetic distribution. The family appears to have diversified greatly with the evolution of the vertebrates, but only a few invertebrate deuterostome TGF-beta molecules have so far been isolated. A search for members of this family expressed in sea urchin embryos, using canonical PCR primers, revealed a single-copy gene encoding a new TGF-beta protein. The sequence which it encodes is closely related to those of vertebrate bone morphogenetic proteins (BMPs) 5-7. No additional TGF-beta family members were uncovered other than univin, which had previously been reported. (+info)
Efficient studies of long-distance Bmp5 gene regulation using bacterial artificial chromosomes. (4/42)The regulatory regions surrounding many genes may be large and difficult to study using standard transgenic approaches. Here we describe the use of bacterial artificial chromosome clones to rapidly survey hundreds of kilobases of DNA for potential regulatory sequences surrounding the mouse bone morphogenetic protein-5 (Bmp5) gene. Simple coinjection of large insert clones with lacZ reporter constructs recapitulates all of the sites of expression observed previously with numerous small constructs covering a large, complex regulatory region. The coinjection approach has made it possible to rapidly survey other regions of the Bmp5 gene for potential control elements, to confirm the location of several elements predicted from previous expression studies using regulatory mutations at the Bmp5 locus, to test whether Bmp5 control regions act similarly on endogenous and foreign promoters, and to show that Bmp5 control elements are capable of rescuing phenotypic effects of a Bmp5 deficiency. This rapid approach has identified new Bmp5 control regions responsible for controlling the development of specific anatomical structures in the vertebrate skeleton. A similar approach may be useful for studying complex control regions surrounding many other genes important in embryonic development and human disease. (+info)
Bone morphogenetic protein-5 (BMP-5) promotes dendritic growth in cultured sympathetic neurons. (5/42)BACKGROUND: BMP-5 is expressed in the nervous system throughout development and into adulthood. However its effects on neural tissues are not well defined. BMP-5 is a member of the 60A subgroup of BMPs, other members of which have been shown to stimulate dendritic growth in central and peripheral neurons. We therefore examined the possibility that BMP-5 similarly enhances dendritic growth in cultured sympathetic neurons. RESULTS: Sympathetic neurons cultured in the absence of serum or glial cells do not form dendrites; however, addition of BMP-5 causes these neurons to extend multiple dendritic processes, which is preceded by an increase in phosphorylation of the Smad-1 transcription factor. The dendrite-promoting activity of BMP-5 is significantly inhibited by the BMP antagonists noggin and follistatin and by a BMPR-IA-Fc chimeric protein. RT-PCR and immunocytochemical analyses indicate that BMP-5 mRNA and protein are expressed in the superior cervical ganglia (SCG) during times of initial growth and rapid expansion of the dendritic arbor. CONCLUSIONS: These data suggest a role for BMP-5 in regulating dendritic growth in sympathetic neurons. The signaling pathway that mediates the dendrite-promoting activity of BMP-5 may involve binding to BMPR-IA and activation of Smad-1, and relative levels of BMP antagonists such as noggin and follistatin may modulate BMP-5 signaling. Since BMP-5 is expressed at relatively high levels not only in the developing but also the adult nervous system, these findings suggest the possibility that BMP-5 regulates dendritic morphology not only in the developing, but also the adult nervous system. (+info)
Expression of bone morphogenetic protein-5 gene during chick heart development: possible roles in valvuloseptal endocardial cushion formation. (6/42)The bone morphogenetic protein (BMP) family, comprising multifunctional peptide growth factors, regulates many developmental processes in a variety of tissues. We examined the spatiotemporal expression of BMP5 by in situ hybridization in chick embryonic hearts from stages 5 to 33. The BMP5 gene was first expressed in the endoderm underlying the precardiac mesoderm at stages 5 to 8. Thereafter, BMP5 expression was restricted to the myocardium of the atrioventricular (AV) canal and outflow tract (OT) regions, where the valvuloseptal endocardial cushion tissue is induced. These results suggest that BMP5 may play important roles not only in myocardial differentiation, but also in the formation and maintenance of endocardial cushion tissue. (+info)
Bone morphogenetic proteins promote cartilage differentiation and protect engineered artificial cartilage from fibroblast invasion and destruction. (7/42)OBJECTIVE: An important role in joint and cartilage homeostasis in adults has been demonstrated recently for morphogenetic factors of the transforming growth factor beta family. Therefore, this study was undertaken to investigate the potential of bone morphogenetic proteins (BMPs) in chondrocyte differentiation using current technologies of tissue engineering. METHODS: Complementary DNAs of recombinant human BMPs 2, 4, 5, 6, and 7 were transfected into primary bovine articular chondrocytes. Transgenic chondrocytes were assembled 3-dimensionally in alginate or in bioresorbable co-polymer fleeces of vicryl and polydioxanon embedded in low-melting-point agarose. Redifferentiation and formation of cartilage tissue in vitro or after subcutaneous transplantation into nude mice were assayed by semiquantitative reverse transcriptase-polymerase chain reaction, histology, and in situ hybridization, and findings were compared with those in unmodified or control-transfected primary chondrocytes. RESULTS: Compared with other BMPs and control vector, BMP-7 induced a decrease in type I collagen expression in artificial cartilage, while transcription of the cartilage-specific type II collagen remained stable. In transplantation experiments, BMP-7 transgenic cartilage revealed the greatest amount of matrix synthesis, and BMP-7 was the only morphogen to suppress the infiltrative response of mouse fibroblastic cells into engineered cartilage, thereby preventing transplant destruction. CONCLUSION: Cartilage differentiation and matrix maturation are promoted by BMPs in cartilage engineering. The inhibitory effect of BMP-7 on a nonspecific infiltrative response in immunocompromised nude mice further suggests that individual morphogens not only may contribute to cartilage maturation, but also may protect it from nonspecific inflammation and invasive destruction. These properties advance BMPs as promising tools for engineering of cartilaginous joint bioprostheses and as candidate biologic agents or genes for cartilage stabilization in arthritis. (+info)
The specification of noradrenergic locus coeruleus (LC) neurones depends on bone morphogenetic proteins (BMPs). (8/42)The role of BMPs in the development of the major noradrenergic centre of the brain, the locus coeruleus (LC), was investigated. LC generation is reflected by initial expression of the transcription factors Phox2a and Phox2b in dorsal rhombomere1 (r1), followed by expression of dopamine-beta-hydroxylase and tyrosine hydroxylase. Bmp5 is expressed in the dorsal neuroepithelium in proximity to Phox2-expressing cells. BMP inhibition in stage 10 chick embryos resulted in the lack of LC neurones or in their generation at the dorsal midline, and loss of roof plate and rhombic lip, but it did not affect neural crest development. These results reveal late essential BMP functions in the specification of dorsal neuronal phenotypes in r1, including LC neurones, and in the development of dorsal midline structures. (+info)
There are several factors that can contribute to bone resorption, including:
1. Hormonal changes: Hormones such as parathyroid hormone (PTH) and calcitonin can regulate bone resorption. Imbalances in these hormones can lead to excessive bone resorption.
2. Aging: As we age, our bones undergo remodeling more frequently, leading to increased bone resorption.
3. Nutrient deficiencies: Deficiencies in calcium, vitamin D, and other nutrients can impair bone health and lead to excessive bone resorption.
4. Inflammation: Chronic inflammation can increase bone resorption, leading to bone loss and weakening.
5. Genetics: Some genetic disorders can affect bone metabolism and lead to abnormal bone resorption.
6. Medications: Certain medications, such as glucocorticoids and anticonvulsants, can increase bone resorption.
7. Diseases: Conditions such as osteoporosis, Paget's disease of bone, and bone cancer can lead to abnormal bone resorption.
Bone resorption can be diagnosed through a range of tests, including:
1. Bone mineral density (BMD) testing: This test measures the density of bone in specific areas of the body. Low BMD can indicate bone loss and excessive bone resorption.
2. X-rays and imaging studies: These tests can help identify abnormal bone growth or other signs of bone resorption.
3. Blood tests: Blood tests can measure levels of certain hormones and nutrients that are involved in bone metabolism.
4. Bone biopsy: A bone biopsy can provide a direct view of the bone tissue and help diagnose conditions such as Paget's disease or bone cancer.
Treatment for bone resorption depends on the underlying cause and may include:
1. Medications: Bisphosphonates, hormone therapy, and other medications can help slow or stop bone resorption.
2. Diet and exercise: A healthy diet rich in calcium and vitamin D, along with regular exercise, can help maintain strong bones.
3. Physical therapy: In some cases, physical therapy may be recommended to improve bone strength and mobility.
4. Surgery: In severe cases of bone resorption, surgery may be necessary to repair or replace damaged bone tissue.
Some common types of bone neoplasms include:
* Osteochondromas: These are benign tumors that grow on the surface of a bone.
* Giant cell tumors: These are benign tumors that can occur in any bone of the body.
* Chondromyxoid fibromas: These are rare, benign tumors that develop in the cartilage of a bone.
* Ewing's sarcoma: This is a malignant tumor that usually occurs in the long bones of the arms and legs.
* Multiple myeloma: This is a type of cancer that affects the plasma cells in the bone marrow.
Symptoms of bone neoplasms can include pain, swelling, or deformity of the affected bone, as well as weakness or fatigue. Treatment options depend on the type and location of the tumor, as well as the severity of the symptoms. Treatment may involve surgery, radiation therapy, chemotherapy, or a combination of these.
Some common types of bone diseases include:
1. Osteoporosis: A condition characterized by brittle, porous bones that are prone to fracture.
2. Osteoarthritis: A degenerative joint disease that causes pain and stiffness in the joints.
3. Rheumatoid arthritis: An autoimmune disorder that causes inflammation and pain in the joints.
4. Bone cancer: A malignant tumor that develops in the bones.
5. Paget's disease of bone: A condition characterized by abnormal bone growth and deformity.
6. Osteogenesis imperfecta: A genetic disorder that affects the formation of bone and can cause brittle bones and other skeletal deformities.
7. Fibrous dysplasia: A rare condition characterized by abnormal growth and development of bone tissue.
8. Multiple myeloma: A type of cancer that affects the plasma cells in the bone marrow.
9. Bone cysts: Fluid-filled cavities that can form in the bones and cause pain, weakness, and deformity.
10. Bone spurs: Abnormal growths of bone that can form along the edges of joints and cause pain and stiffness.
Bone diseases can be diagnosed through a variety of tests, including X-rays, CT scans, MRI scans, and bone biopsies. Treatment options vary depending on the specific disease and can include medication, surgery, or a combination of both.
Heterotopic ossification can cause a range of symptoms depending on its location and severity, including pain, stiffness, limited mobility, and difficulty moving the affected limb or joint. Treatment options for heterotopic ossification include medications to reduce inflammation and pain, physical therapy to maintain range of motion, and in severe cases, surgical removal of the abnormal bone growth.
In medical imaging, heterotopic ossification is often diagnosed using X-rays or other imaging techniques such as CT or MRI scans. These tests can help identify the presence of bone growth in an abnormal location and determine the extent of the condition.
Overall, heterotopic ossification is a relatively rare condition that can have a significant impact on a person's quality of life if left untreated. Prompt medical attention and appropriate treatment can help manage symptoms and prevent long-term complications.
Example Sentence: The patient was diagnosed with pulmonary hypertension and began treatment with medication to lower her blood pressure and improve her symptoms.
Word class: Noun phrase / medical condition
The exact cause of myositis ossificans is not fully understood, but it is thought to be related to an abnormal repair process within the muscle tissue. The condition can be diagnosed through a combination of physical examination, imaging studies such as X-rays or MRIs, and biopsy.
Treatment for myositis ossificans usually focuses on relieving pain and improving mobility. This may include rest, physical therapy, anti-inflammatory medications, and in some cases, surgery to remove the abnormal bone growth. The condition can take several months to resolve, and in rare cases, it may recur.
Myositis ossificans is a relatively rare condition, but it can have a significant impact on an individual's quality of life, particularly if left untreated. It is important for healthcare providers to be aware of this condition and its symptoms in order to provide accurate diagnosis and appropriate treatment.
* American Academy of Orthopaedic Surgeons. (2019). Myositis Ossificans. Retrieved from
* MedlinePlus. (2020). Myositis ossificans. Retrieved from
* UW Health. (n.d.). Myositis Ossificans. Retrieved from
Open fracture: The bone breaks through the skin, exposing the bone to the outside environment.
Closed fracture: The bone breaks, but does not penetrate the skin.
Comminuted fracture: The bone is broken into many pieces.
Hairline fracture: A thin crack in the bone that does not fully break it.
Non-displaced fracture: The bone is broken, but remains in its normal position.
Displaced fracture: The bone is broken and out of its normal position.
Stress fracture: A small crack in the bone caused by repetitive stress or overuse.
* Osteogenesis imperfecta (OI): A genetic disorder that affects the formation of bone tissue, leading to fragile bones and an increased risk of fractures.
* Rickets: A vitamin D-deficient disease that causes softening of the bones in children.
* Osteomalacia: A condition similar to rickets, but affecting adults and caused by a deficiency of vitamin D or calcium.
* Hyperparathyroidism: A condition in which the parathyroid glands produce too much parathyroid hormone (PTH), leading to an imbalance in bone metabolism and an increase in bone resorption.
* Hypoparathyroidism: A condition in which the parathyroid glands produce too little PTH, leading to low levels of calcium and vitamin D and an increased risk of osteoporosis.
Bone diseases, metabolic are typically diagnosed through a combination of physical examination, imaging studies such as X-rays or CT scans, and laboratory tests to evaluate bone metabolism. Treatment depends on the specific underlying cause of the disease and may include medications, dietary changes, or surgery.
Note: The medical information provided here is for general purposes only and should not be considered a substitute for professional medical advice, diagnosis, or treatment. If you suspect that your child may have a congenital limb deformity, it is important to consult with a qualified healthcare provider as soon as possible.
There are two types of brachydactyly:
1. Postaxial brachydactyly: This type affects the little finger side of the hand, causing the corresponding finger to be shorter than the others.
2. Preaxial brachydactyly: This type affects the thumb side of the hand, causing the corresponding finger to be shorter than the others.
Brachydactyly can be caused by a variety of genetic mutations or chromosomal abnormalities, such as Turner syndrome, Noonan syndrome, and Down syndrome. It can also be caused by environmental factors, such as maternal diabetes during pregnancy.
The symptoms of brachydactyly may include:
* Shortened fingers or toes
* Limited range of motion in the affected digits
* Difficulty grasping or manipulating objects
* Aesthetic concerns
Treatment for brachydactyly depends on the underlying cause and severity of the condition. In some cases, surgery may be necessary to lengthen the affected fingers or toes. Physical therapy and occupational therapy can also help improve range of motion and function.
It's important to note that brachydactyly is usually a congenital condition, meaning it is present at birth. However, in some cases, it may not be diagnosed until later in childhood or adulthood. If you suspect your child or yourself may have brachydactyly, it's important to consult with a healthcare professional for proper evaluation and treatment.
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
There are different types of fractures that can occur in cartilage, including:
1. Fissure fractures: These are small cracks or splits in the cartilage.
2. Fracture-linear fractures: These are longer, more linear cracks in the cartilage.
3. Fracture-bucket handle fractures: These are fractures that have a central crack with two smaller cracks radiating from it, resembling a bucket handle.
4. Fracture-segmental fractures: These are fractures that involve the entire thickness of the cartilage and can be complete or incomplete.
Fractures, cartilage can be caused by a variety of factors, including trauma, sports injuries, degenerative conditions such as osteoarthritis, and systemic diseases such as rheumatoid arthritis. Symptoms of fractures, cartilage can include pain, stiffness, limited mobility, and locking or catching sensations in the affected joint.
Diagnosis of fractures, cartilage is typically made through a combination of physical examination, imaging studies such as X-rays, CT scans, and MRI, and arthroscopy, which involves inserting a small camera into the joint to visualize the cartilage directly.
Treatment for fractures, cartilage depends on the severity of the injury and can include conservative measures such as rest, physical therapy, and medication, or surgical interventions such as repair or replacement of the damaged cartilage. In severe cases, fractures, cartilage may require joint fusion or replacement with an artificial joint.
There are several types of osteoporosis, including:
1. Postmenopausal osteoporosis: This type of osteoporosis is caused by hormonal changes that occur during menopause. It is the most common form of osteoporosis and affects women more than men.
2. Senile osteoporosis: This type of osteoporosis is caused by aging and is the most common form of osteoporosis in older adults.
3. Juvenile osteoporosis: This type of osteoporosis affects children and young adults and can be caused by a variety of genetic disorders or other medical conditions.
4. secondary osteoporosis: This type of osteoporosis is caused by other medical conditions, such as rheumatoid arthritis, Crohn's disease, or ulcerative colitis.
The symptoms of osteoporosis can be subtle and may not appear until a fracture has occurred. They can include:
1. Back pain or loss of height
2. A stooped posture
3. Fractures, especially in the spine, hips, or wrists
4. Loss of bone density, as determined by a bone density test
The diagnosis of osteoporosis is typically made through a combination of physical examination, medical history, and imaging tests, such as X-rays or bone density tests. Treatment for osteoporosis can include medications, such as bisphosphonates, hormone therapy, or rANK ligand inhibitors, as well as lifestyle changes, such as regular exercise and a balanced diet.
Preventing osteoporosis is important, as it can help to reduce the risk of fractures and other complications. To prevent osteoporosis, individuals can:
1. Get enough calcium and vitamin D throughout their lives
2. Exercise regularly, especially weight-bearing activities such as walking or running
3. Avoid smoking and excessive alcohol consumption
4. Maintain a healthy body weight
5. Consider taking medications to prevent osteoporosis, such as bisphosphonates, if recommended by a healthcare provider.
1. Skull deformities: Synostosis can lead to abnormal growth and shape of the skull, which can cause visual disturbances, hearing loss, and other complications.
2. Respiratory problems: Fused bones in the skull can reduce the size of the nasal passages and sinuses, making it harder to breathe properly.
3. Neurological issues: Synostosis can press on the brain and spinal cord, leading to headaches, seizures, and other neurological symptoms.
4. Vision problems: The fusion of bones can cause double vision or other visual disturbances, which can affect a child's ability to learn and develop normally.
5. Hearing loss: In some cases, synostosis can lead to hearing loss due to the abnormal growth of the bones in the middle ear.
6. Sleep apnea: Synostosis can cause the airway to be narrowed or blocked, leading to sleep apnea and other breathing problems.
7. Dental problems: Fused bones in the skull can affect the alignment of teeth and lead to dental problems such as crowding, misalignment, or tooth loss.
8. Speech difficulties: Synostosis can cause speech difficulties due to the abnormal growth of the bones in the mouth and throat.
9. Feeding difficulties: Fused bones in the skull can make it harder for a child to eat properly, leading to feeding difficulties and malnutrition.
10. Emotional and social challenges: Children with synostosis may experience emotional and social challenges due to their appearance or difficulty with basic functions such as eating and breathing.
Treatment for synostosis usually involves a combination of surgery, physical therapy, and other supportive care to help manage the symptoms and improve quality of life.
There are several different types of calcinosis, each with its own unique causes and symptoms. Some common forms of calcinosis include:
1. Dystrophic calcinosis: This type of calcinosis occurs in people with muscular dystrophy, a group of genetic disorders that affect muscle strength and function. Dystrophic calcinosis can cause calcium deposits to form in the muscles, leading to muscle weakness and wasting.
2. Metastatic calcinosis: This type of calcinosis occurs when cancer cells spread to other parts of the body and cause calcium deposits to form. Metastatic calcinosis can occur in people with a variety of different types of cancer, including breast, lung, and prostate cancer.
3. Idiopathic calcinosis: This type of calcinosis occurs for no apparent reason, and the exact cause is not known. Idiopathic calcinosis can affect people of all ages and can cause calcium deposits to form in a variety of different tissues.
4. Secondary calcinosis: This type of calcidosis occurs as a result of an underlying medical condition or injury. For example, secondary calcinosis can occur in people with kidney disease, hyperparathyroidism (a condition in which the parathyroid glands produce too much parathyroid hormone), or traumatic injuries.
Treatment for calcinosis depends on the underlying cause and the severity of the condition. In some cases, treatment may involve managing the underlying disease or condition that is causing the calcium deposits to form. Other treatments may include medications to reduce inflammation and pain, physical therapy to improve mobility and strength, and surgery to remove the calcium deposits.
The tumor is typically made up of compact, densely packed osteoblastic cells that resemble normal bone tissue. However, unlike normal bone tissue, osteoblastoma has a markedly increased number of blood vessels and can be quite large before it penetrates the surrounding bone.
The exact cause of osteoblastoma is not known, but it is believed to arise from genetic mutations that occur during fetal development. There are several types of osteoblastoma, including:
* Cartilage-forming osteoblastoma: This type of tumor is composed of both osteoblastic and chondrocytic cells and is typically found in the long bones of the arms and legs.
* Fibrous dysplasia: This is a related condition that also arises from abnormalities in the development of bone, but it is not classified as a tumor.
Osteoblastoma is usually diagnosed with imaging tests such as X-rays, CT scans, or MRI scans, and a biopsy may be performed to confirm the diagnosis. Treatment typically involves surgery to remove the tumor, followed by radiation therapy to prevent recurrence. In rare cases, the tumor may be malignant and require more aggressive treatment.
Prognosis for osteoblastoma is generally good if the tumor is diagnosed and treated early, but it can be challenging to distinguish benign from malignant tumors based on imaging studies alone. Therefore, biopsy and careful follow-up are essential to ensure that any recurrences are detected and treated promptly.
The alveolar bone is a specialized type of bone that forms the socket in which the tooth roots are embedded. It provides support and stability to the teeth and helps maintain the proper position of the teeth in their sockets. When the alveolar bone is lost, the teeth may become loose or even fall out completely.
Alveolar bone loss can be detected through various diagnostic methods such as dental X-rays, CT scans, or MRI scans. Treatment options for alveolar bone loss depend on the underlying cause and may include antibiotics, bone grafting, or tooth extraction.
In the context of dentistry, alveolar bone loss is a common complication of periodontal disease, which is a chronic inflammatory condition that affects the supporting structures of the teeth, including the gums and bone. The bacteria that cause periodontal disease can lead to the destruction of the alveolar bone, resulting in tooth loss.
In addition to periodontal disease, other factors that can contribute to alveolar bone loss include:
* Trauma or injury to the teeth or jaw
* Poorly fitting dentures or other prosthetic devices
* Infections or abscesses in the mouth
* Certain systemic diseases such as osteoporosis or cancer
Overall, alveolar bone loss is a significant issue in dentistry and can have a major impact on the health and function of the teeth and jaw. It is essential to seek professional dental care if symptoms of alveolar bone loss are present to prevent further damage and restore oral health.
There are several types of bone cysts, including:
1. Simple bone cysts: These are the most common type of bone cyst and typically occur in children and young adults. They are filled with air or fluid and do not contain any cancerous cells.
2. Angiomatous cysts: These are smaller than simple bone cysts and are usually found near the ends of long bones. They are also filled with blood vessels and do not contain any cancerous cells.
3. Unicameral (simple) bone cysts: These are similar to simple bone cysts but are larger and may be more complex in shape.
4. Multicameral bone cysts: These are larger than unicameral bone cysts and may contain multiple chambers filled with air or fluid.
5. Enchondromas: These are benign tumors that occur within the cartilage of a bone. They are usually found in the long bones of the arms and legs.
6. Chondromyxoid fibromas: These are rare, benign tumors that occur in the cartilage of a bone. They are typically found in the long bones of the arms and legs.
7. Osteochondromas: These are benign tumors that arise from the cartilage and bone of a joint. They are usually found near the ends of long bones.
8. Malignant bone cysts: These are rare and can be cancerous. They may occur in any bone of the body and can be aggressive, spreading quickly to other areas of the body.
The symptoms of bone cysts can vary depending on their size and location. They may cause pain, swelling, and limited mobility in the affected limb. In some cases, they may also lead to fractures or deformities.
Diagnosis of bone cysts usually involves imaging tests such as X-rays, CT scans, or MRI scans. A biopsy may also be performed to confirm the diagnosis and rule out other possible conditions.
Treatment for bone cysts depends on their size, location, and severity. Small, asymptomatic cysts may not require any treatment, while larger cysts may need to be drained or surgically removed. In some cases, medication such as bisphosphonates may be used to help reduce the risk of fractures.
In conclusion, bone cysts are abnormalities that can occur in any bone of the body. They can be benign or malignant and can cause a range of symptoms depending on their size and location. Diagnosis is usually made through imaging tests, and treatment may involve observation, draining, or surgical removal.
Synonyms: cartilage tumor, chondroid tumor, chondromatosis.
Etymology: From the Greek words "chondros," meaning cartilage, and "oma," meaning tumor.
Examples of Chondroma in a sentence:
1. The patient was diagnosed with a chondroma in their knee joint, which was causing pain and stiffness.
2. The surgeon removed the chondroma from the patient's lung, which had been compressing the bronchus and causing difficulty breathing.
3. The chondroma in the patient's heart was monitored with regular imaging studies to ensure it did not grow or cause any further complications.
4. The patient was advised to avoid heavy lifting or bending to prevent exacerbating their chondroma in the spine.
Tibial fractures can range in severity from minor cracks or hairline breaks to more severe breaks that extend into the bone's shaft or even the joint. Treatment for these injuries often involves immobilization of the affected leg with a cast, brace, or walking boot, as well as pain management with medication and physical therapy. In some cases, surgery may be necessary to realign and stabilize the bone fragments.
Note: A malunited fracture is sometimes also referred to as a "nonunion fracture" or "fracture nonunion".
The word "holoprosencephaly" comes from the Greek words "holos," meaning "whole," "prosencephalon," meaning "front part of the brain," and "-ly," indicating a condition or characteristic. The term was first used in the medical literature in the late 19th century to describe this specific type of brain malformation.
In individuals with holoprosencephaly, the two hemispheres of the brain do not properly separate, leading to various abnormalities and impairments. Depending on the severity and location of the defect, symptoms can range from mild to severe and may include:
1. Facial abnormalities, such as a single eye or no nose.
2. Cognitive impairments, including intellectual disability and developmental delays.
3. Motor difficulties, such as weakness or paralysis on one side of the body.
4. Seizures and other neurological problems.
5. Delayed speech and language development.
6. Behavioral challenges, including autism and anxiety.
The exact cause of holoprosencephaly is not fully understood, but it is thought to be related to genetic mutations or environmental factors during early fetal development. Diagnosis is typically made through a combination of prenatal imaging, such as ultrasound or MRI, and postnatal examination, including physical examination and neuroimaging studies.
There is no standard treatment for holoprosencephaly, and management of the condition usually involves a multidisciplinary approach involving neurosurgeons, neurologists, developmental pediatricians, and other specialists. Treatment may include surgery to correct physical abnormalities, medication to control seizures or other neurological symptoms, and various forms of therapy to address cognitive, motor, and behavioral challenges.
The prognosis for holoprosencephaly varies depending on the severity of the condition and the presence of any additional birth defects or medical issues. Some individuals with holoprosencephaly may have a relatively mild form of the condition and can lead active, fulfilling lives with appropriate support and management, while others may experience significant cognitive and physical challenges that require ongoing care and support.
Some common types of eye abnormalities include:
1. Refractive errors: These are errors in the way the eye focuses light, causing blurry vision. Examples include myopia (nearsightedness), hyperopia (farsightedness), astigmatism, and presbyopia (age-related loss of near vision).
2. Amblyopia: This is a condition where the brain favors one eye over the other, causing poor vision in the weaker eye.
3. Cataracts: A cataract is a clouding of the lens in the eye that can cause blurry vision and increase the risk of glaucoma.
4. Glaucoma: This is a group of eye conditions that can damage the optic nerve and lead to vision loss.
5. Macular degeneration: This is a condition where the macula, the part of the retina responsible for central vision, deteriorates, leading to vision loss.
6. Diabetic retinopathy: This is a complication of diabetes that can damage the blood vessels in the retina and lead to vision loss.
7. Retinal detachment: This is a condition where the retina becomes separated from the underlying tissue, leading to vision loss.
8. Corneal abnormalities: These are irregularities in the shape or structure of the cornea, such as keratoconus, that can cause blurry vision.
9. Optic nerve disorders: These are conditions that affect the optic nerve, such as optic neuritis, that can cause vision loss.
10. Traumatic eye injuries: These are injuries to the eye or surrounding tissue that can cause vision loss or other eye abnormalities.
Eye abnormalities can be diagnosed through a comprehensive eye exam, which may include visual acuity tests, refraction tests, and imaging tests such as retinal photography or optical coherence tomography (OCT). Treatment for eye abnormalities depends on the specific condition and may include glasses or contact lenses, medication, surgery, or other therapies.
People with HHT have abnormal blood vessels in their skin, mucous membranes, and organs such as the liver, spleen, and lungs. These abnormal vessels are weak and prone to bleeding, which can lead to nosebleeds, bruising, and other complications.
HHT is usually diagnosed based on a combination of clinical symptoms and genetic testing. Treatment typically involves managing symptoms with medications, lifestyle changes, and in some cases, surgery or other interventions to prevent bleeding episodes.
Some of the main symptoms of HHT include:
* Recurring nosebleeds
* Easy bruising
* Petechiae (tiny red spots on the skin)
* Purpura (larger purple spots on the skin)
* Gingival bleeding (bleeding from the gums)
* Epistaxis (nosebleeds)
* Hematuria (blood in the urine)
* Gastrointestinal bleeding
HHT is a relatively rare disorder, affecting about 1 in 5,000 to 1 in 10,000 people worldwide. It can be inherited in an autosomal dominant pattern, meaning that a single copy of the mutated gene is enough to cause the condition. However, some cases may be caused by spontaneous mutations and not be inherited.
There are several types of HHT, including:
* Type 1: The most common type, characterized by recurring nosebleeds and other bleeding episodes.
* Type 2: Characterized by a milder form of the condition with fewer bleeding episodes.
* Type 3: A rare and severe form of HHT that is often associated with other medical conditions such as liver disease or pulmonary hypertension.
HHT can be diagnosed based on clinical findings and laboratory tests, including:
* Physical examination: To look for signs of bleeding and to assess the size and shape of the nose and ears.
* Imaging studies: Such as CT or MRI scans to evaluate the nasal passages and sinuses.
* Blood tests: To check for abnormalities in blood clotting and platelet function.
* Genetic testing: To identify mutations in the genes associated with HHT.
Treatment for HHT is focused on managing symptoms and preventing complications. It may include:
* Nasal decongestants and antihistamines to reduce bleeding and swelling.
* Corticosteroids to reduce inflammation.
* Antifibrinolytic medications to prevent blood clots from breaking down.
* Surgery to repair or remove affected blood vessels.
* Regular monitoring of blood counts and platelet function.
Early diagnosis and treatment can help improve the quality of life for people with HHT. It is important to seek medical attention if symptoms persist or worsen over time.
The exact cause of osteoarthritis is not known, but it is thought to be due to a combination of factors such as genetics, wear and tear on joints over time, and injuries or trauma to the joint. Osteoarthritis can affect any joint in the body, but it most commonly affects the hands, knees, hips, and spine.
The symptoms of osteoarthritis can vary depending on the severity of the condition and which joint is affected. Common symptoms include:
* Pain or tenderness in the joint
* Stiffness, especially after periods of rest or inactivity
* Limited mobility or loss of flexibility
* Grating or crackling sensations when the joint is moved
* Swelling or redness in the affected joint
* Muscle weakness or wasting
There is no cure for osteoarthritis, but there are several treatment options available to manage the symptoms and slow the progression of the disease. These include:
* Pain relief medications such as acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs)
* Physical therapy to improve mobility and strength
* Lifestyle modifications such as weight loss, regular exercise, and avoiding activities that exacerbate the condition
* Bracing or orthotics to support the affected joint
* Corticosteroid injections or hyaluronic acid injections to reduce inflammation and improve joint function
* Joint replacement surgery in severe cases where other treatments have failed.
Early diagnosis and treatment of osteoarthritis can help manage symptoms, slow the progression of the disease, and improve quality of life for individuals with this condition.
There are several types of osteosarcomas, including:
1. High-grade osteosarcoma: This is the most common type of osteosarcoma and tends to grow quickly.
2. Low-grade osteosarcoma: This type of osteosarcoma grows more slowly than high-grade osteosarcoma.
3. Chondrosarcoma: This is a type of osteosarcoma that arises in the cartilage cells of the bone.
4. Ewing's family of tumors: These are rare types of osteosarcoma that can occur in any bone of the body.
The exact cause of osteosarcoma is not known, but certain risk factors may increase the likelihood of developing the disease. These include:
1. Previous radiation exposure
2. Paget's disease of bone
3. Li-Fraumeni syndrome (a genetic disorder that increases the risk of certain types of cancer)
4. Familial retinoblastoma (a rare inherited condition)
5. Exposure to certain chemicals, such as herbicides and industrial chemicals.
Symptoms of osteosarcoma may include:
1. Pain in the affected bone, which may be worse at night or with activity
2. Swelling and redness around the affected area
3. Limited mobility or stiffness in the affected limb
4. A visible lump or mass on the affected bone
5. Fractures or breaks in the affected bone
If osteosarcoma is suspected, a doctor may perform several tests to confirm the diagnosis and determine the extent of the disease. These may include:
1. Imaging studies, such as X-rays, CT scans, or MRI scans
2. Biopsy, in which a sample of tissue is removed from the affected bone and examined under a microscope for cancer cells
3. Blood tests to check for elevated levels of certain enzymes that are produced by osteosarcoma cells
4. Bone scans to look for areas of increased activity or metabolism in the bones.
There are several types of hypertrophy, including:
1. Muscle hypertrophy: The enlargement of muscle fibers due to increased protein synthesis and cell growth, often seen in individuals who engage in resistance training exercises.
2. Cardiac hypertrophy: The enlargement of the heart due to an increase in cardiac workload, often seen in individuals with high blood pressure or other cardiovascular conditions.
3. Adipose tissue hypertrophy: The excessive growth of fat cells, often seen in individuals who are obese or have insulin resistance.
4. Neurological hypertrophy: The enlargement of neural structures such as brain or spinal cord due to an increase in the number of neurons or glial cells, often seen in individuals with neurodegenerative diseases such as Alzheimer's or Parkinson's.
5. Hepatic hypertrophy: The enlargement of the liver due to an increase in the number of liver cells, often seen in individuals with liver disease or cirrhosis.
6. Renal hypertrophy: The enlargement of the kidneys due to an increase in blood flow and filtration, often seen in individuals with kidney disease or hypertension.
7. Ovarian hypertrophy: The enlargement of the ovaries due to an increase in the number of follicles or hormonal imbalances, often seen in individuals with polycystic ovary syndrome (PCOS).
Hypertrophy can be diagnosed through various medical tests such as imaging studies (e.g., CT scans, MRI), biopsies, and blood tests. Treatment options for hypertrophy depend on the underlying cause and may include medications, lifestyle changes, and surgery.
In conclusion, hypertrophy is a growth or enlargement of cells, tissues, or organs in response to an excessive stimulus. It can occur in various parts of the body, including the brain, liver, kidneys, heart, muscles, and ovaries. Understanding the underlying causes and diagnosis of hypertrophy is crucial for effective treatment and management of related health conditions.
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HELENE COPPIN - IRSD
- 8. Smad1/5 and Smad4 expression are important for osteoclast differentiation. (nih.gov)
- 12. Smad 1/5 is involved in bone morphogenetic protein-2-induced odontoblastic differentiation in human dental pulp cells. (nih.gov)
- 14. Endoglin is involved in BMP-2-induced osteogenic differentiation of periodontal ligament cells through a pathway independent of Smad-1/5/8 phosphorylation. (nih.gov)
- The transforming growth factor-beta (TGF-β) superfamily includes TGF-β isoforms, activins/inhibins, nodal, anti-Müllerian hormone proteins, growth differentiation factors (GDFs), and bone morphogenetic proteins (BMPs), which play critical roles in embryogenesis and adult tissue homeostasis. (nature.com)
- These data set up that at least one effect of ALK2 gain-of-function mutations in FOP individuals is definitely enhanced chondrogenic differentiation which helps formation of heterotopic endochondral bone. (bioshockinfinitereleasedate.com)
- The Alk2R206H gain-of-function mutation enhances both canonical (phospho-Smad1/5/8) and noncanonical (phophop38) BMP signaling reactions in the absence of ligand [17 18 23 Furthermore lesion biopsies from FOP individuals and a R206H knockin mouse model exposed that cartilage differentiation happens within regions of fibroproliferation [2 10 11 26 The induction of chondrogenesis is definitely therefore an important early step in the pathology of FOP. (bioshockinfinitereleasedate.com)
- Normal physiological levels of GCs are essential for development, metabolism, normal osteoblast differentiation, and bone formation. (biomedcentral.com)
- Enhanced secretion of proteins specific for differentiation toward bone as well as calcium deposition and alkaline phosphatase activity were observed in irradiated cells cultured in a medium not supplemented with osteogenic factors. (class4lasers.com)
- 15. Activation of the bone morphogenetic protein signaling pathway induces inhibin beta(B)-subunit mRNA and secreted inhibin B levels in cultured human granulosa-luteal cells. (nih.gov)
- This facilitates activation of the neighboring protein kinase website that consequently induces downstream transmission transduction by phosphorylating BMP-specific Smads (Smad1 Smad5 and Smad8) and/or components of the mitogen-activated protein kinase (MAPK) pathway to regulate gene transcription . (bioshockinfinitereleasedate.com)
- Bone morphogenic protein is an isolated protein that induces specific cells in our body to form new cartilage and bone. (maxsurg.com)
- 3. Transforming growth factor β inhibits bone morphogenetic protein-induced transcription through novel phosphorylated Smad1/5-Smad3 complexes. (nih.gov)
- 9. Transforming growth factor-β1 suppresses bone morphogenetic protein-2-induced mesenchymal-epithelial transition in HSC-4 human oral squamous cell carcinoma cells via Smad1/5/9 pathway suppression. (nih.gov)
- Of note, treatment with GIP, but not treatment with GLP-1, augmented Smad1/5/8 phosphorylation and transcription of the BMP target gene Id-1 induced by BMP-6 stimulation, suggesting that GIP upregulates BMP receptor signaling that can inhibit FSH-induced progesterone synthesis in rat granulosa cells. (elsevierpure.com)
- Recent advances in extracellular signaling suggest that extracellular protein phosphorylation is a regulatory mechanism outside the cell. (biomedcentral.com)
- The list of reported active extracellular protein kinases and phosphatases is growing, and phosphorylation of an increasing number of extracellular matrix molecules and extracellular domains of trans-membrane proteins is being documented. (biomedcentral.com)
- Here, we use public proteomic databases, collagens - the major components of the extracellular matrix, extracellular signaling molecules and proteolytic enzymes as examples to assess what the roles of extracellular protein phosphorylation may be in health and disease. (biomedcentral.com)
- We propose that novel tools be developed to help assess the role of extracellular protein phosphorylation and translate the findings for biomedical applications. (biomedcentral.com)
- Technical advances have significantly contributed to insights into the functional role of extracellular protein phosphorylation. (biomedcentral.com)
- In principle, phosphorylation of secretory proteins could happen prior to secretion or in the extracellular matrix (ECM). (biomedcentral.com)
- Alterations in phosphorylation of secreted proteins during their transit through the secretory pathway might interfere with their folding, transport, secretion, release from the cell surface or interaction with other ECM components. (biomedcentral.com)
- Phosphorylation and dephosphorylation events in the ECM may regulate the processing, assembly, degradation and binding properties of matrix proteins. (biomedcentral.com)
- In any case, the widespread phosphorylation of extracellular matrix proteins suggests that the mechanism of reversible protein phosphorylation may not only be a mechanism inside cells as widely demonstrated, but may also be a regulatory mechanism outside cells. (biomedcentral.com)
- One protein in the SIBLING group, osteopontin (OPN), inhibits HA formation, and this inhibition depends on the degree of phosphorylation [ 25 ]. (biomedcentral.com)
- 13. Inhibition of mTORC1 kinase activates Smads 1 and 5 but not Smad8 in human prostate cancer cells, mediating cytostatic response to rapamycin. (nih.gov)
- How important such kinase activity maybe for the functions of extracellular proteins is well illustrated by evidence that mutations in secreted kinases can lead to severe disorders. (biomedcentral.com)
- Our previous studies have demonstrated that insulin signaling pathway has an important role in the pathophysiology of polycystic ovary syndrome (PCOS), including phosphatidylinositol 3-kinase and protein kinase B signaling, which is critically implicated in insulin resistance, androgen secretion, obesity, and follicular development. (intechopen.com)
- The HJV gene provides instructions for making a protein called hemojuvelin. (medlineplus.gov)
- Most HJV gene mutations change one of the protein building blocks (amino acids) used to make hemojuvelin. (medlineplus.gov)
- Mutations in the HJV gene lead to an altered hemojuvelin protein that cannot function properly. (medlineplus.gov)
- gene which encodes ALK2 a type I bone morphogenetic protein (BMP) receptor [5 6 12 Most FOP individuals possess the same specific R206H substitution in ALK2. (bioshockinfinitereleasedate.com)
- Meanwhile, 5-AZA-dC suppressed the increase in MGMT and MLH1 gene methylation in osteoblasts treated with low doses of NaF, leading to enhanced expression of MGMT and MLH1 mRNA. (fluoridealert.org)
- The abnormal methylation of the mismatch repair gene MLH1 can lead to the transcriptional inactivation of mRNA and the loss of protein expression , which will result in defects in the mismatch repair function of the body, thus causing instability of the whole genome and eventually leading to the occurrence of tumours [ 9 ]. (fluoridealert.org)
- Evaluation of the association between a single-nucleotide polymorphism of bone morphogenetic proteins 5 gene and risk of knee osteoarthritis. (cdc.gov)
- The kisspeptin, which is the product of the gene and KISS1 stimulates gonadotropin-releasing hormone (GnRH), which binds to a receptor coupled to G (GPR54) protein, which stimulates the release of GnRH by hypothalamic neurons, leading to the secretion of pituitary gonadotropins LH and FSH and sex steroids which in turn will act on the gonads to produce gametes. (fapesp.br)
- Germline mutations of the gene encoding bone morphogenetic protein receptor ( BMPR ) type 2 are certainly clear examples of established risk factors for PAH development 4 . (ersjournals.com)
- Bone morphogenetic proteins (BMPs) are a group of growth factors also known as cytokines and as metabologens.Originally discovered by their ability to induce the formation of bone and cartilage, BMPs are now considered to constitute a group of pivotal morphogenetic signals, orchestrating tissue architecture throughout the body. (fremontobserver.com)
- 2. Bone morphogenetic protein 2 regulates cell-cell communication by down-regulating connexin43 expression in luteinized human granulosa cells. (nih.gov)
- Autologous transplantation with bone marrow-mesenchymal stem cells (BMSCs) could be a promising therapeutical approach but its effect on toxic chemical-induced neuropathy remains undetermined. (researchsquare.com)
- After the development of characteristic phenotypes, rats were given a single bolus tail-vein injection of BMSCs (5×10 7 cells/kg) and followed-up for 5 weeks. (researchsquare.com)
- What are the most promising anabolic targets (cells, ligands/receptors, intracellular signaling pathways) for diseases and disorders of bone, cartilage, and muscle at this time? (nih.gov)
- Samples (1 x10(6) cells/ml) from irradiated and non-irradiated cells of each cell line were incubated with or without 5 microg/ml of Fas ligand peptide for 2 h at 37 degrees C in a humidified atmosphere of 5% carbon dioxide (CO2) in air. (nih.gov)
- As the sponge dissolves, the bone morphogenic protein stimulates the cells to produce new bone. (maxsurg.com)
- Aggregated mesenchymal cells at the defect, chondrocytes at the hypertrophic cartilage, and osteoblasts adjunct to newly formed woven bone showed intensive proliferating cell nuclear antigen expression. (tmu.edu.tw)
- Mesenchymal stem cells (MSCs) are multipotent cells capable of differentiating into several tissues, such as bone, cartilage, and fat. (biomedcentral.com)
- Taken together these findings indicate that laser treatment enhances the in vitro proliferation of Saos-2 cells, and also influences their osteogenic maturation, which suggest it is a helpful application for bone tissue regeneration. (class4lasers.com)
- 5-HT levels are known to be elevated in PAH 12 and 5-HT acts as growth factor for pulmonary artery smooth muscle cells 13 , 14 , thus possibly contributing to the pathophysiology of PAH development and progression. (ersjournals.com)
- Fas antigen, also termed APO-1 or CD95, is a transmembrane protein and a member of the tumor necrosis factor receptor/nerve growth factor receptor superfamily which mediates apoptosis upon oligomerization. (nih.gov)
- Nine (22.5%) out of 40 patients evaluated resulted positive for the presence of germline bone morphogenetic protein receptor ( BMPR) type 2 mutations. (ersjournals.com)
- Bone morphogenetic protein signaling by hemojuvelin regulates hepcidin expression. (medlineplus.gov)
- Furthermore, the DNA methyltransferase inhibitor 5-AZA-dC suppressed cell viability , cell number in S-phase, ALP activity and osteogenesis-related protein levels in osteoblasts treated with low doses of NaF. (fluoridealert.org)
- In osteoblasts treated with NaF, excessive methylation of p16 has been reported to be induced, causing increased cell proliferation , prolonged S-phase of the cell cycle, and skeletal fluorosis progression, while the methylation inhibitor 5-aza-2-deoxycytidine (5-AZA-dC) reverses the hypermethylation of p16 induced by NaF [ 6 ]. (fluoridealert.org)
- Evidence for its role in cartilage formation can be seen in MICE , where genetic mutations that cause loss of bone morphogenetic protein 5 function result in the formation of small malformed ears. (nih.gov)
- Other mutations create a premature stop signal in the instructions for making the hemojuvelin protein resulting in an abnormally small protein. (medlineplus.gov)
- Mutations in KRIT1, a protein initially identified based on a yeast two-hybrid interaction with the RAS-family GTPase RAP1A, are responsible for the development of the inherited vascular disorder cerebral cavernous malformations (CCM1). (nih.gov)
- It is a potent regulator of the growth of CHONDROCYTES and the synthesis of cartilage matrix proteins. (nih.gov)
- Purification of bovine bone morphogenetic protein by hydroxyapatite chromatography. (bvsalud.org)
- Arosarena O.A., Collins W.L. Bone regeneration in the rat mandible with bone morphogenetic protein-2: a comparison of two carriers. (genescells.ru)
- ESW treatment significantly promoted BMP-2, BMP-3, BMP-4, and BMP-7 mRNA expression of callus as determined by RT-PCR, and BMP immunoreactivity appeared throughout the bone regeneration period. (tmu.edu.tw)
- Our findings suggest that BMP play an important role in signaling ESW-activated cell proliferation and bone regeneration of segmental defect. (tmu.edu.tw)
- Several studies have shown that low-level laser irradiation (LLLI) has beneficial effects on bone regeneration. (class4lasers.com)
- Death of bone marrow occurs within 6-12 hours after vascular insult. (medscape.com)
- Platelet-derived extracellular vesicles infiltrate and modify the bone marrow during inflammation. (harvard.edu)
- Glucocorticoid-induced osteonecrosis and osteoporosis are caused by various factors including dysfunction of bone marrow MSCs. (biomedcentral.com)
- 1999 May;64(5):1388-93. (medlineplus.gov)
- The GR is an intracellular protein that is ubiquitously expressed in almost every cell of the organism and interacts with chromatin to modulate the activity of numerous transcription factors in a cell type-specific manner. (biomedcentral.com)
- [ 5 ] Studies have also shown elevated cryofibrinogen levels in atraumatic osteonecrosis. (medscape.com)
- In this paper we show that application of bone morphogenetic protein rhBMP-2 in demineralized cancellous bone blocks provides great improving osteoinductivity of the material in the ectopic model subcutaneous implantation in rats. (genescells.ru)
- The model of ectopic subcutaneous implantation to rats is very convenience test system to detect increase in osteoinductivity of materials caused by application of rhBMP-2, and to identify features of ectopic bone formation in these materials. (genescells.ru)
- Low-level laser therapy enhances the expression of osteogenic factors during bone repair in rats. (class4lasers.com)
- The aim of this study was to evaluate the effects of low-level laser therapy (LLLT) on bone formation, immunoexpression of osteogenic factors, and biomechanical properties in a tibial bone defect model in rats. (class4lasers.com)
- Sixty male Wistar rats were distributed into bone defect control group (CG) and laser irradiated group (LG). (class4lasers.com)
- At present, novel osteoinductive materials containing recombinant bone morphogenetic proteins (rhBMPs) are actively being developed for «regenerative medicine», traumatology and orthopedics. (genescells.ru)
- A treatment for FOP and anemia of inflammation, as well as BMP driven diseases (certain cancers, cardio-vascular disease, inflammation, hematological disease and bone disorders). (nih.gov)
- Sickle cell anemia results in bone death secondary to the sickling process and subsequent vascular occlusion. (medscape.com)
- Research and Clinical Studies that Support Bone Healing and Osteogenesis with Laser Therapy Treatments. (class4lasers.com)
- Alkaline phosphatase (ALP) was calculated to evaluate bone formation and turnover. (fluoridealert.org)
- Bone lesions of skeletal fluorosis are complicated and varied, due mainly to the destruction of bone formation and bone resorption balance and the acceleration of bone turnover [ 1 ]. (fluoridealert.org)
- mRNA and protein expression levels were assessed using qRT-PCR and Western blot assays. (fluoridealert.org)
- abstract = " Extracorporeal shock wave (ESW) is a noninvasive acoustic wave, which has recently been demonstrated to promote bone repair. (tmu.edu.tw)
- Abstract Objective: The therapeutic outcomes of low-level laser therapy (LLLT) on closed bone fractures (CBFs) in the wrist and hand were investigated in this controlled study. (class4lasers.com)
- The participants agreed that strategies for activating anabolic pathways in bone, cartilage, and muscle hold considerable potential to yield new therapeutic approaches for diseases relating to individual tissues and for the musculoskeletal system as a whole. (nih.gov)
- If fluoride is taken in large amounts over a long period of time, fluoride can cause abnormal proliferation and activation of osteoblasts and osteoclasts , leading to skeletal fluorosis, which can lead to pain and damage to joints and bones and even permanent disability [ 3 , 5 ]. (fluoridealert.org)
- In a previous study of this subject, the osteoblasts of primary cultured mice were found to always proliferate when the fluoride dose was 5-20 mg/L, and the proliferation of osteoblasts was the highest when the fluoride dose was 10 mg/L (preliminary research on this subject). (fluoridealert.org)
- A bone morphogenetic protein that may play a role in CARTILAGE formation. (nih.gov)
- This establishes ALK2 like a plausible restorative target during early chondrogenic phases of lesion formation for avoiding heterotopic bone formation in FOP and additional conditions. (bioshockinfinitereleasedate.com)
- Also, a higher amount of newly formed bone was observed at 15 days postsurgery. (class4lasers.com)
- Diisocyanates are the most common cause of occupational asthma from low-molecular weight chemicals, still causing disease in 5-15 % of chronically exposed workers despite improved industrial hygiene efforts. (cdc.gov)
- They reviewed what is known about anabolic processes of bone, cartilage, and muscle, and progress toward developing anabolic therapies for related disorders. (nih.gov)
- Hemojuvelin and bone morphogenetic protein (BMP) signaling in iron homeostasis. (medlineplus.gov)
- Description: A competitive ELISA for quantitative measurement of Human Bone morphogenetic protein 8A(BMP8A) in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. (isogem.org)
- McKay W.F., Peckham S.M., Badura J.M. A comprehensive clinical review of recombinant human bone morphogenetic protein-2 (INFUSE Bone Graft). (genescells.ru)
- From parallel screens of human fetal brain and HeLa cDNA libraries, we obtained multiple independent isolates of human integrin cytoplasmic domain-associated protein-1 (ICAP-1) as interacting clones. (nih.gov)
- however, little research has been conducted to determine the effect of LLLT on the treatment of human bone fractures. (class4lasers.com)
- A fragment containing the N-terminal 272 amino acid residues of KRIT1, a region lacking similarity to any known protein upon database searches, was used as bait. (nih.gov)
- The participants noted that, while the bone, cartilage, and muscle fields are at different stages of research and therapeutic development, all would benefit from additional studies. (nih.gov)
- As the function of the KRIT1 protein and its role in CCM pathogenesis remain unknown, we performed yeast two-hybrid screens to identify additional protein binding partners. (nih.gov)
- Description: A sandwich ELISA kit for detection of Bone Morphogenetic Protein 8A from Rat in samples from blood, serum, plasma, cell culture fluid and other biological fluids. (isogem.org)